Spatiotemporal control of cAMP signalling processes by anchored signalling complexes

被引：67

作者：

Jarnaess, E. ^{[1
]}

Tasken, K. ^{[1
]}

机构：

[1] Univ Oslo, Biotechnol Ctr Oslo, N-0317 Oslo, Norway

来源：

BIOCHEMICAL SOCIETY TRANSACTIONS | 2007年 / 35卷

关键词：

A-kinase-anchoring protein (AKAP); cAMP; compartmentalization; extracellular-signal-regulated kinase (ERK); phosphodiesterase (PDE); protein kinase A (PKA);

D O I：

10.1042/BST0350931

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Ligand-induced changes in cAMP concentration vary in duration, amplitude and extension into the cell. cAMP microdomains are shaped by adenylate cyclases that form cAMP as well as PDEs (phosphodiesterases) that degrade cAMP. Various extracellular signals converge on the cAMP/PKA (protein kinase A) pathway through ligand binding to GPCRs (G-protein-coupled receptors) and the cAMP/PKA pathway is therefore tightly regulated on several levels to maintain specificity in the multitude of signal inputs. AKAPs (A-kinase-anchoring proteins) target PKA to specific substrates and distinct subcellular compartments, providing spatial and temporal specificity for mediation of biological effects channelled through the cAMP/PKA pathway. AKAPs also serve as scaffolding proteins that assemble PKA together with signal terminators such as phosphoprotein phosphatases and cAMP-specific PDEs as well as components of other signalling pathways into multiprotein signalling complexes.

引用

页码：931 / 937

页数：7

共 48 条

[1] Bioinformatic design of A-kinase anchoring protein-in silico:: A potent and selective peptide antagonist of type II protein kinase A anchoring [J].